Management of pregnancies complicated by anti-Fy(a) alloimmunization

BACKGROUND: The objective was to evaluate the management and outcome of patients with anti-Fy(a) at the Ohio State University. STUDY DESIGN AND METHODS: A database search for patients with pregnancies complicated only by anti-Fy(a) from 1959 to 2004. Collected information included maternal testing, fetal therapy, and neonatal outcomes. RESULTS: The final data set included 18 pregnancies in 15 women where anti-Fy(a) was the only maternal alloantibody present and the fetus was Fy(a) antigen-positive. Maternal antibody titers of at least 32 and optical density at 450 nm values in modified Liley Zone IIB or III identified all fetuses or neonates with significant hemolytic disease (2/18, 11%). No fetuses had hydrops, and there were no deaths attributed to hemolytic disease of the fetus and newborn. CONCLUSION: Anti-Fy(a) has the potential to lead to significant fetal hemolysis. Management guidelines developed for D sensitization are appropriate for pregnancies complicated by anti-Fy(a) alloimmunization.     

Activation of human dendritic cells by p-phenylenediamine

Exposure to p-phenylenediamine (pPD), a primary intermediate in hair dye formulations, is often associated with the development of allergic contact dermatitis. Such reactions involve activation of the subject's immune system. The aim of these studies was to explore the relationship between pPD oxidation and functional maturation of human monocyte-derived dendritic cells in vitro. Dendritic cells were incubated with pPD and Bandrowski's base (BB) for 16 h, and expression of the costimulatory receptors CD40, CD80, CD83, CD86, and major histocompatibility complex class II intracellular glutathione levels and cell viability were measured. In certain experiments, glutathione (1 mM) was added to culture medium. Liquid chromatography-mass spectrometry (LC-MS) analysis and exhaustive solvent extraction were used to monitor the rate of [(14)C]pPD oxidation and the extent of pPD binding to cellular and serum protein, respectively. Proliferation of allogeneic lymphocytes was determined by incorporation of [(3)H]thymidine. Exposure of dendritic cells to pPD (5-50 microM), but not BB, was associated with an increase in CD40 and MHC class II expression and proliferation of allogeneic lymphocytes. Dendritic cell activation with pPD was not associated with apoptotic or necrotic cell death or depletion of glutathione. Neither pPD nor BB altered dendritic cell expression of CD80, CD83, or CD86. LC-MS analysis revealed pPD was rapidly oxidized in cell culture media to BB. Addition of glutathione inhibited BB formation but did not prevent covalent binding of pPD to dendritic cell protein or dendritic cell activation. Collectively, these studies show that pPD, but not BB, selectively activates human dendritic cells in vitro.     

New onset diabetes with ketoacidosis attributed to quetiapine

A 45-year-old man with paranoid schizophrenia with delusions was transferred from a group home for treatment of diabetic ketoacidosis (DKA). Six months before this episode, he had been hospitalized in an inpatient psychiatric institution and treated with valproic acid and quetiapine 400 mg with normal blood sugars recorded. The patient was treated for diabetic ketoacidosis, and all outpatient medications were discontinued. Insulin resistance is commonly cited as the mechanism for hyperglycemia, a theory supported by the efficacy of insulin- sensitizing medications in reported cases. Although antipsychotic- associated DKA is uncommon, hyperglycemia associated with these medications is commonplace. Analysis of case series have not identified risk factors for hyperglycemia or diabetic ketoacidosis within this population. Considering the incidence and unpredictability of hyperglycemia associated with quetiapine and atypical antipsychotics, clinicians should initiate intensive monitoring in patients, including weight, hyperglycemia, and dyslipidemia.     

Studying sex and gender differences in pain and analgesia: a consensus report

In September 2006, members of the Sex, Gender and Pain Special Interest Group of the International Association for the Study of Pain met to discuss the following: (1) what is known about sex and gender differences in pain and analgesia; (2) what are the "best practice" guidelines for pain research with respect to sex and gender; and (3) what are the crucial questions to address in the near future? The resulting consensus presented herein includes input from basic science, clinical and psychosocial pain researchers, as well as from recognized experts in sexual differentiation and reproductive endocrinology. We intend this document to serve as a utilitarian and thought-provoking guide for future research on sex and gender differences in pain and analgesia, both for those currently working in this field as well as those still wondering, "Do I really need to study females?"